Heart failure (HF) is a chronic disease afflicting millions of Americans and others around the world. HF refers generally to a disease condition characterized by a reduced capacity of the heart to effectively pump blood. HF is generally a progressive condition for which there is currently no known cure. The only currently known way to eliminate heart failure is with a heart transplant, however, the number of patients which may benefit from a heart transplant procedure far outnumber the quantity of available hearts for transplant. A variety of pharmacological therapies are known however which can ameliorate or suppress HF symptoms in certain patients.
HF is often coincident with one or more cardiac arrhythmia conditions, and thus some HF patients may be provided with a cardiac rhythm management device, such as an implantable pacemaker which may be combined with an implantable cardioverter defibrillator (ICD). For certain patients, appropriate multi-chamber low voltage pacing stimulation can improve cooperation between the multiple chambers of the heart and restore a degree of pumping effectiveness lost due to HF. ICDs provide relatively high energy/high voltage therapeutic shocks to interrupt episodes of fibrillation or to defibrillate the patient.
Pacing stimulations and defibrillation shocks are delivered via implanted electrodes which are arranged in contact with or near the patient's cardiac tissue. Electrodes can be positioned internally within the heart and such electrodes are often transvenously introduced. Electrodes can also be affixed in the exterior surface of the heart or configured as conductive external structures of implanted stimulation pulse generator/controller units. Surface electrodes have also been considered to apply stimulation to larger exterior surfaces of the patient's heart. Surface electrodes have proven difficult to implement as it has proven problematic to reliably maintain surface electrodes in a desired position over time. The heart exterior undergoes rather significant motion throughout the cardiac cycle and this motion tends to dislodge electrodes and electrode fixations positioned on the surface.
One further physiological characteristic of certain HF patients and one more commonly found in more severe conditions of HF is an excessive distention or dilation of the heart. The heart normally expands and contracts throughout the cardiac cycle about a median stable size. However, in certain patients as the HF progresses, the heart can become abnormally enlarged or dilated such that the overall size of the heart is greater than in a pre-disease normal condition. Unfortunately, this excessive dilation or distention strains and weakens the heart and reduces its pumping capacity, thus requiring even more exertion from the weakened diseased heart. The over-exertion of the heart required to maintain the pumping output of the heart can further weaken the cardiac tissue leading to further dilation or distention of the heart muscle in a positive feedback progression of the chronic HF condition.
One proposed therapy for HF patients experiencing heart dilation is to provide some sort of mechanical or structural support to the heart muscle to resist excessive enlargement of the heart. For example, a variety of structures known generally as cardiac constraints have been proposed to partially encompass the outer surface of the heart to limit excessive distention of a diseased heart. While such cardiac constraints do not halt the progression of the HF, it appears that in certain cases they may be able to offer benefits in limiting the progression of continued heart enlargement and weakening of the heart muscle during heart failure-based dilation.